Notably, glioblastoma plasticity (Figure S3B) [18], EMT (Figure S3C) [19], tumorigenesis (Figure S3F) [20], tumor anaplastic (Figure S3D) [21], gliomagenesis by platelet derived growth factor B (PDGFB) (Figure S3A) [22], cancer metastasis signature (Figure S3E) [23], common cancer genes (Figure S3G) [24], targets of PTCH1 and SUFU (Figure S3H) and several other gene sets were remarkably enriched in the TACC3 high group, which confirmed the oncogenic role of TACC3 in tumor progression and partially uncovered the potential mechanism (Table S7). Here, SUFU is linked to neoplasm.